NUCLEIC ACIDS RESEARCH, ISSN 0305-1048, 07/2019, Volume 47, Issue W1, pp. W308 - W314
Disulfide bonds play a significant role in protein stability, function or regulation but are poorly conserved among evolutionarily related proteins. The Yosshi...
CHAIN | DESIGN | STABILITY | STABILIZATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | BOND | TOOL | Web Server Issue
CHAIN | DESIGN | STABILITY | STABILIZATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | BOND | TOOL | Web Server Issue
Journal Article
Journal of Bioinformatics and Computational Biology, ISSN 0219-7200, 04/2018, Volume 16, Issue 2
The visualCMAT web-server was designed to assist experimental research in the fields of protein/enzyme biochemistry, protein engineering, and drug discovery by...
binding sites | functionally diverse families and superfamilies | Correlated mutations/co-evolving residues | structure-function relationship | physically interacting correlated pairs | allosteric regulation | long-range correlations | protein design | web-server | COEVOLUTION | SPECIFICITY | STABILITY | CONTACT PREDICTION | INFORMATION-THEORETIC ANALYSIS | EVOLUTION | SEQUENCE ALIGNMENT | MATHEMATICAL & COMPUTATIONAL BIOLOGY | SITES | STRUCTURE PREDICTION | COMMUNICATION
binding sites | functionally diverse families and superfamilies | Correlated mutations/co-evolving residues | structure-function relationship | physically interacting correlated pairs | allosteric regulation | long-range correlations | protein design | web-server | COEVOLUTION | SPECIFICITY | STABILITY | CONTACT PREDICTION | INFORMATION-THEORETIC ANALYSIS | EVOLUTION | SEQUENCE ALIGNMENT | MATHEMATICAL & COMPUTATIONAL BIOLOGY | SITES | STRUCTURE PREDICTION | COMMUNICATION
Journal Article
Journal of the American Chemical Society, ISSN 0002-7863, 03/2016, Volume 138, Issue 8, pp. 2563 - 2570
The abnormal overexpression of the BCL2 gene is associated with many human tumors. We found a new 28-mer G-quadruplex-forming sequence, P1G4, immediately...
BREAST-CANCER | CELLS | MAJOR G-QUADRUPLEX | DNA | PROTEIN EXPRESSION | GENE-EXPRESSION | INHIBITOR | CHEMISTRY, MULTIDISCIPLINARY | K+ SOLUTION | REGION | FAMILY | Genetic transcription | Research
BREAST-CANCER | CELLS | MAJOR G-QUADRUPLEX | DNA | PROTEIN EXPRESSION | GENE-EXPRESSION | INHIBITOR | CHEMISTRY, MULTIDISCIPLINARY | K+ SOLUTION | REGION | FAMILY | Genetic transcription | Research
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Targeting FGFR overcomes EMT-mediated resistance in EGFR mutant non-small cell lung cancer
ONCOGENE, ISSN 0950-9232, 09/2019, Volume 38, Issue 37, pp. 6399 - 6413
Evolved resistance to tyrosine kinase inhibitor (TKI)-targeted therapies remains a major clinical challenge. In epidermal growth factor receptor (EGFR) mutant...
MULTIPLE-MYELOMA | GEFITINIB | METASTASIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACQUIRED-RESISTANCE | CELL BIOLOGY | TO-MESENCHYMAL TRANSITION | MET AMPLIFICATION | ONCOLOGY | PATHWAY | GENETICS & HEREDITY | GROWTH-FACTOR RECEPTOR-3 | INHIBITOR | ACTIVATING MUTATIONS | Tyrosine | CRISPR | Fibroblast growth factor | Cell survival | Epidermal growth factor receptors | Small cell lung carcinoma | Mesenchyme | Lung cancer | Non-small cell lung carcinoma | Genomes | Gene expression | Drug resistance | Kinases | Epidermal growth factor | Motivation | Cell lines | Growth factors | Fibroblast growth factor receptor 1 | Protein-tyrosine kinase | Fibroblast growth factor receptors
MULTIPLE-MYELOMA | GEFITINIB | METASTASIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACQUIRED-RESISTANCE | CELL BIOLOGY | TO-MESENCHYMAL TRANSITION | MET AMPLIFICATION | ONCOLOGY | PATHWAY | GENETICS & HEREDITY | GROWTH-FACTOR RECEPTOR-3 | INHIBITOR | ACTIVATING MUTATIONS | Tyrosine | CRISPR | Fibroblast growth factor | Cell survival | Epidermal growth factor receptors | Small cell lung carcinoma | Mesenchyme | Lung cancer | Non-small cell lung carcinoma | Genomes | Gene expression | Drug resistance | Kinases | Epidermal growth factor | Motivation | Cell lines | Growth factors | Fibroblast growth factor receptor 1 | Protein-tyrosine kinase | Fibroblast growth factor receptors
Journal Article
Cancer Research, ISSN 0008-5472, 07/2016, Volume 76, Issue 14 Supplement, pp. 2130 - 2130
Journal Article
Cancer Research, ISSN 0008-5472, 07/2017, Volume 77, Issue 13 Supplement, pp. 2163 - 2163
Journal Article
Journal of bioinformatics and computational biology, 04/2018, Volume 16, Issue 2, p. 1840005
The visualCMAT web-server was designed to assist experimental research in the fields of protein/enzyme biochemistry, protein engineering, and drug discovery by...
Journal Article
Cancer Discovery, ISSN 2159-8274, 06/2018, Volume 8, Issue 6, pp. 714 - 729
The cornerstone of treatment for advanced ALK-positive lung cancer is sequential therapy with increasingly potent and selective ALK inhibitors. The...
EML4-ALK | DRUG-COMBINATIONS | GENE | ONCOLOGY | CERITINIB | OVERCOMES CRIZOTINIB RESISTANCE | ALECTINIB | ACQUIRED-RESISTANCE | OPEN-LABEL | ROS1 | CHEMOTHERAPY | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | Lung Neoplasms - chemically induced | Humans | Ethylnitrosourea - adverse effects | Drug Resistance, Neoplasm | Lactams, Macrocyclic - pharmacology | Anaplastic Lymphoma Kinase - genetics | Whole Exome Sequencing | Xenograft Model Antitumor Assays | Protein Kinase Inhibitors - administration & dosage | Animals | Oncogene Proteins, Fusion - genetics | Crizotinib - pharmacology | Cell Line, Tumor | Crizotinib - administration & dosage | Female | Lactams, Macrocyclic - administration & dosage | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Index Medicus | ALK | brigatinib | crizotinib | lorlatinib | and NSCLC | Anaplastic lymphoma kinase | ceritinib | acquired resistance | alectinib
EML4-ALK | DRUG-COMBINATIONS | GENE | ONCOLOGY | CERITINIB | OVERCOMES CRIZOTINIB RESISTANCE | ALECTINIB | ACQUIRED-RESISTANCE | OPEN-LABEL | ROS1 | CHEMOTHERAPY | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | Lung Neoplasms - chemically induced | Humans | Ethylnitrosourea - adverse effects | Drug Resistance, Neoplasm | Lactams, Macrocyclic - pharmacology | Anaplastic Lymphoma Kinase - genetics | Whole Exome Sequencing | Xenograft Model Antitumor Assays | Protein Kinase Inhibitors - administration & dosage | Animals | Oncogene Proteins, Fusion - genetics | Crizotinib - pharmacology | Cell Line, Tumor | Crizotinib - administration & dosage | Female | Lactams, Macrocyclic - administration & dosage | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Index Medicus | ALK | brigatinib | crizotinib | lorlatinib | and NSCLC | Anaplastic lymphoma kinase | ceritinib | acquired resistance | alectinib
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 01/2019, Volume 25, Issue 2, pp. 796 - 807
Purpose: KRAS-mutant lung cancers have been recalcitrant to treatments including those targeting the MAPK pathway. Covalent inhibitors of KRAS p.G12C allele...
CELL LUNG-CANCER | MUTANT | MEK INHIBITION | ONCOLOGY | SELUMETINIB PLUS DOCETAXEL | RAS | TRAMETINIB | RESISTANCE | ADDICTION
CELL LUNG-CANCER | MUTANT | MEK INHIBITION | ONCOLOGY | SELUMETINIB PLUS DOCETAXEL | RAS | TRAMETINIB | RESISTANCE | ADDICTION
Journal Article
Cancer Discovery, ISSN 2159-8274, 10/2019, p. CD-18-0830
Journal Article
Cancer discovery, ISSN 2159-8274, 12/2018, Volume 8, Issue 12, pp. 1598 - 1613
BH3 mimetic drugs, which inhibit pro-survival BCL-2 family proteins, have limited single-agent activity in solid tumor models. The potential of BH3 mimetics...
Journal Article
Cancer Discovery, ISSN 2159-8274, 12/2018, Volume 8, Issue 12, pp. 1598 - 1613
BH3 mimetic drugs, which inhibit prosurvival BCL2 family proteins, have limited single-agent activity in solid tumor models. The potential of BH3 mimetics for...
DRUG-COMBINATIONS | MEK INHIBITION | ONCOLOGY | BIM | RESISTANCE | REGULATORS | BH3 MIMETIC ABT-737 | PROTEINS | EXPRESSION | DOCETAXEL | TRAMETINIB GSK1120212
DRUG-COMBINATIONS | MEK INHIBITION | ONCOLOGY | BIM | RESISTANCE | REGULATORS | BH3 MIMETIC ABT-737 | PROTEINS | EXPRESSION | DOCETAXEL | TRAMETINIB GSK1120212
Journal Article
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